Ladies and gentlemen, thank you for standing by. Welcome to Compugen's Fourth Quarter and Full Year 2020 Results Conference Call. At this time, all participants are in a listen-only mode. An audio webcast of this call is available in the Investors section of Compugen's website, www.cgen.com. As a reminder, today's call is being recorded. I would now like to introduce Elana Holzman, Compugen's Director of Investor Relations and Corporate Communications. Please go ahead.

Thank you, operator, and thank you for joining us today. With me from Compugen are Dr. Anat Cohen-Dayag, President and CEO; Dr. Henry Adewoye, Chief Medical Officer; Ari Krashin, CFO and COO; and Dr. Eran Ophir, VP, Research and Drug Discovery. Anat will provide corporate highlights, after which Henry will review the data we disclosed earlier today, and Ari will review our financial statement and position. Anat, Henry, Ari and Eran will be available for the Q&A session. Before we begin, I would like to read the following regarding forward-looking statement. During the course of this conference call, the company may make projections or other forward-looking statements regarding future events or future business outlook, our development efforts and their outcomes, anticipated progress and the timeline of our programs, financial and accounting-related matters, as well as statements regarding our cash position. We wish to caution you that such statements reflect only the company's current expectations and that actual events or results may differ materially. You are kindly referred to the risk factors and cautionary language contained in the documents the company filed with the Securities and Exchange Commission including the company's most recent Annual Report filed on Form 20-F with the Securities and Exchange Commission. The company undertakes no obligation to update projections or forward-looking statements in the future. I will now turn the call over to Anat. Anat?

Thank you, Elana. Good morning and good afternoon, everyone, and welcome to our fourth quarter and full year 2020 corporate and financial update. 2020 was another important year of execution and progress of Compugen, in which we strengthened our positioning in the cancer immunotherapy space and solidified our standing as the leader in targeting DNAM axis signaling pathways. Based on our years of research of this axis, we are executing a strategic and comprehensive clinical development program to evaluate our internally discovered and wholly-owned anti-PVRIG and TIGIT assets across settings and combination regimens to elucidate the role of the DNAM axis members, PVRIG and TIGIT as potentially foundational immunotherapy checkpoint targets. Our work has identified PVRIG and TIGIT as key parallel and complementary inhibitory pathways in the DNAM axis, which also intersects with the PD1 pathway. Importantly, our data suggest that these three inhibitory pathways have different dominance in different tumor types and patient populations, which means certain patient populations may require the blockade of different combinations of the three pathways in order to induce effective anti-tumor immune responses. This is the underlying rationale for our comprehensive clinical program designed to develop new treatment solutions. Earlier today, we shared data from the combination arm of the Phase 1 dose escalation study of COM701 in combination with Bristol-Myers Squibb's nivolumab, as well as follow-up on our monotherapy dose escalation study and data from the COM701 monotherapy cohort expansion. While Henry will provide a more detailed review of the data later in the call, I would like to present a high level overview of our data and highlight certain results, which we view as particularly encouraging. We plan to present updated data, along with initial relative data from patient samples at ASCO 2021 to which an abstract was submitted. Starting with the…

Thank you, Anat, and good day to everyone. As Anat reviewed this morning, we disclosed data from a combination arm of COM701 with nivolumab and COM701 monotherapy expansion cohorts. In April of 2020 at AACR, we reported data in patients enrolled with the dose escalation arms of the ongoing Phase 1 study of COM701 monotherapy in combination with nivolumab in patients with advanced solid tumors. This included data from all monotherapy dose escalation cohorts through 20 milligrams per kilogram IV Q four weeks and four of the five dose levels from the dual combination dose escalation arm. We were encouraged we’ve booked the preliminary acceptable safety and tolerability profile and preliminary antitumor activity of COM701 monotherapy and in combination with nivolumab. Notably, there were two durable partial responses. One partial response in the combination arm of the patients with colorectal cancer as microsatellite stable, which treatment is ongoing for more than ten months. Typically, patients with colorectal cancer that has MSS are unresponsive to immune checkpoint inhibitors and published data demonstrates the median PFS of approximately eight weeks in this patient population. We reported another partial response in the monotherapy arm of a patient with primary peritoneal cancer that is also platinum-resistant and with microsatellite stable status with treatment ongoing at 24 weeks at the time of the presentation. Overall, we were encouraged with the durability of antitumor activity and responses with the number of patients in the combination arm remaining on study for over 200 days. I can share that when we reported dose-limiting toxicities in dose level 5 of the dual combination dose escalation arm of COM701 20 milligrams per kilogram one way plus nivolumab 42 milligrams for IV Q four weeks and the remaining is to be finding have been dosed. Additionally, the PK profile of COM701…

Thank you, Henry. Good morning and good afternoon to everyone. Our financial results for the fourth quarter and the full year of 2020 released this morning reflect the continued expenses associated with our ongoing various clinical programs. Our revenue for the fourth quarter and full year of 2020 were $2 million, representing the first development milestone from our license agreement with AstraZeneca announced during the fourth quarter. Research and development expenses during the full year of 2020 were $22.8 million, an increase of approximately 15%, compared with $19.8 million in 2019. For the fourth quarter of 2020, research and development expenses were $8.1 million, an increase of 88%, compared with $4.3 million in the prior year period of 2019. The increase in both cases is attributed mostly to higher clinical studies, related expenses, as well as CMC related activities, specifically manufacturing for additional drug supply of both COM701 and COM902 to support the planned expansion of our various clinical trials. Net loss for the full year of 2020 was $29.7 million or $0.37 per basic and diluted share, compared with a net loss of $27.3 million or $0.43 per basic and diluted share for 2019. Net loss for the fourth quarter of 2020 was $8.6 million or $0.10 per basic and diluted share, compared with a net loss of $6.5 million or $0.10 per basic and diluted share for the prior year period. As of December 31, 2020, we had approximately $124 million in cash and cash-related accounts, compared with approximately $44 million at the end of the prior year. We have no debt. The increase in our cash balances is mostly attributed to approximately $74 million of net proceeds received in our public offering last March, approximately $18 million received from exercise of warrants and approximately $16 million received from exercise of employee options offset by operating expenses and working capital of approximately $28 million. Going into 2021, we expect to have gross cash expenditures to be in the range between $40 million to $42 million without taking into consideration any potential cash inflows for the company from existing or new collaboration. Thank you. And with that, we will now open the call for questions.

[Operator Instructions] The first question is from Chris Howerton of Jefferies. Please go ahead.

Hey, good morning, and thanks for taking the questions. So, I guess, first of all, obviously great to see another complete response. But I guess, I am curious about the monotherapies arms, what, at least by your eyes, the expansion cohort seem to have at least flatter or slightly less efficacy. So, I am curious to see Henry or Anat what your explanations might be in terms of what could explain the differences between those two patient populations or subjects in those two different study arms? So, that’s one question. The second question would be, with respect to the CR it’s such a low dosage of 0.3 mg, what do you think is going on there? And then I guess that is kind of tacking on to my third question, which is how – could you give us a little more color on kind of the biomarker strategy? And how is it that you are going to try and elucidate what is it, like prospectively, what are the tumor types or patients that could respond to mono, double or triple therapies? Thank you.

Sure. Hi, Chris. And I’ll start by just a few remarks and then I’ll turn to Henry answer the questions. But I think that in general for the monotherapy, we are trying not to compare it to portions of the studies with different patients, et cetera, we look at the totality of the data and the directionality of the data that we generated, the dose escalation as well as the monotherapy expansion. I’ll let Henry related to the CR and then we’ll get back to the biomarker strategy. Henry?

Yes. Thank you very much, Anat. And thank you very much for your questions, Chris. Yes, we looked at the data also, but the key takeaway from what I would like to say here is that, the two different ways to look at this data and you’ll come to the same conclusion and the conclusion you’ll come to is there is preliminary antitumor activity with COM701 monotherapy and also in combination with nivolumab. And if you were to look at the dose escalation cohorts, the objective of that of the study was just to establish what the safety and tolerability profile and DLTs with COM701 starting at a very low dose. For the expansion cohort, the primary objective of this cohort was simply to establish what the safety and tolerability of COM701 is at the recommended dose for expansion which is 20 mg per kilogram body weight IV Q 4 weeks. So we’ve been able to demonstrate this from what we’ve been able to show and therefore that’s the only assessment one should be able to take from it. And in addition remember that in patients who are also on therapy on the COM701 20 mg per kilogram body weight dose, we have highlighted that at least a third of those patients, right, 6 out of the 20 have stable disease during the course of the – in my prepared remarks. So, that’s the way we will look at it and it will be very, very difficult to start comparing dose escalation with DLTs as an endpoints with safety and tolerability in the expansion cohorts, even though you do still see the same antitumor activity for both. Right. So, let me go to the second question with the confirmed complete response. Yes, so, remember, Chris, that we presented data at…

Yes. No. That’s really helpful. And then, so, I guess, with respect to the CR, basically the – I mean, my assumption with respect to the biology is there was obviously some escape with respect to nivolumab’s mechanism of action and that the 75% receptor occupancy you feel is enough to get the blockade of the rest of the pathway I guess is kind of the message you are saying, Henry?

Yes. But remember, the receptor occupancy, I am talking about is peripheral. It’s not within the tumor. And therefore –yes, and therefore, please remember again that the reason we went – the dose that was selected is because of the patient population that we intend to explore. That’s one. And then number two, one of the patients having 20 mg per kilogram body weight dose that’s the patient that has a tumor type that is typically unresponsive to immune checkpoints and that’s the patient with primary peritoneal cancer. At the very first assessment for that patient, the patient had a partial response. We presented that patient data and the images that were captured by the investigator at AACR last year, so the partial response actually different with 20 mg per kilogram body weight dose. And that patient has held on to that response for than a year now. So, it shows that you probably within the tumor cells, and especially in patients who have been treated previously with checkpoints or several lines of chemotherapy, you will need to achieve sufficient penetration into the tumor itself. The other patient I would like to bring up also that is also pertinent, the patient with microsatellite stable colorectal cancer, it’s the same thing that we observed in that patient. Remember, that was the patient that we presented also at AACR and for that patient the – that patient had four prior lines of treatment and the way on COM701 on the combination of nuvo – nuvo was 360 mg IV Q 3 weeks and COM701was 0.3 mg per kilogram body weight dose. That patient was on study treatment and confirmed stable disease up until about seven months before he didn’t had any PR, partial response that then was confirmed several times afterwards. So that’s the totality and the interpretation of that data.

All right. That’s great. I don’t know, Anat, if you wanted to add anything to Henry’s comments with respect to the biomarker strategy, but I appreciate the response.

Yes. Sure. Yes, yes. I would just add, I’ll let Eran related to the biomarker strategy, but I would just say that just in terms of looking at the totality of the data and that will be of the monotherapy and that will be a segue to the biomarker discussion. And we also stated that we see immune activation in our initial correlative assessments in that sample and that’s in the single agent and also in combination. And I think that when you look at the story of what’s the antitumor activity when you look at the totality of the data, as well as the fact that there was immune activation, any different tumor types and durable antitumor activity. For us, it serves as the basis in order to take it to the next page. We think that the data points to the fact that COM701 is active. We will continue to look at the monotherapy setting. That patient is still on study. We will continue to do some additional correlation studies, additional biomarker work related and will make the decisions with respect to monotherapy specifically as we have the full data. But now, it serves us well in order to move forward into the combinations and to expand our strategy for a combination treatment. So, Eran, would you like to relate to the biomarker?

Yes. So, as already mentioned, you are looking at the pre and post samples. We are looking at the expression of the DNAM axis, try to correlate response with the expression of the axis. We are looking at the immuno durable activity of COM701. We do that by looking at peripheral blood and we already expected today that you see that’s COM701 probably enhance immunity, which is very important to see. And then, other than, we are also going to look at tumor microenvironment with different sequences methods to try to see a modulation of tumor microenvironment in addition to what we already see in peripheral blood by COM701 and by that we’ll try to link all of it with response and indication and patient selection.

Got it. Okay. And the pre post biopsy analyses, particularly for the DNAM axis, is that anticipated to be at ASCO this year, Eran?

At this stage, we stated that initial correlative assessments would be presented - in general will be presented at ASCO if we are accepted. We didn’t give guidance yet to the DNAM axis biomarkers, immuno histochemistry. This is work in progress and we’ll for sure share the data, but didn’t give guidance yet.

Okay. Okay. Well, wonderful to see the progress and again, thank you very much for taking the questions and your answers.

Thank you.

The next question is from Stephen Willey of Stifel. Please go ahead.

Yes. Good morning. Thanks for taking the question and I was jumping around a bit. So, forgive me if I ask something that was already discussed. But, can you maybe just provide a little bit more color around the kinetics of the CR patients in the doublet cohort? How long was that patients confirmed to have stable disease before they flipped to CR? And I guess I ask the question, because I know that there is three other patients who are still in the midst of confirmed stable disease for some pretty long durations and I am just trying to get a sense as to whether or not those patients could also become responders at some point based upon the kinetics of the CR that was observed.

Henry, I guess, you will take it.

Yes, yes. I will. Hi, Steve. So, the patients with the confirmed complete response with enough squamous cell carcinoma was bound study treatment for nine months until we observed the complete response. And I think that the complete response, like I mentioned has not been confirmed repeatedly.

Okay. And for those remaining patients that are on – that are still in the midst of a confirmed stable disease, I guess, for six plus months. Are those patients also at a 20 mg per kg dose? Have you been able to dose escalate those patients as you cleared in various dose levels or have you kept those patients at their pre-specified dose level?

Yes. So, for those patients who were at the dose escalation for both the monotherapy and for the combination dose escalation, with the exception of first two dose cohorts, there was no intra subject dose escalation. So, they will remain at the doses that they are on if they are still on the study. So for example, the patients that are at the 20 mg per kg body weight dose with pancreatic cancer, which we have in addition that’s ongoing at that dose in the dose, that patient will remain at that dose. So we can collect safety and tolerability. But the previous data we disclosed, we didn’t had any dose – dose escalation , what, for one patient, which was at a very, very low dose at that point.

Okay. And then, have you mentioned or can you discuss at this point, I guess, how many patients you are intending to enroll with each of the doublet dose expansion cohorts? Should we anticipate that this is going to be kind of like monotherapy dose expansion where you had a small number of patients over kind of a fairly heterogeneous selection of tumor types? Or should we expect more patient numbers to be represented by each tumor type?

So, we give – go ahead, Henry.

Yes. So, we - if you go and link with trials.gov, we do say there for the expansion cohort, the dual combination. We don’t have more patients. So, remember, for the monotherapy expansion, we only had 4 patients per tumor type. We have five tumor types, lung, ovarian, breast, endometrial and colorectal which is microsatellite stable colorectal. For the expansion cohorts for the dual combination will have more patients up to about 20 patients in several tumor types that are of interest to us.

Okay. So you’ll have up to 20 patients on a per tumor type basis?

That is correct.

Okay. And then, I believe there is plans also to look at COM701 with 902. I guess, is that a correct assumption? And in pursuing that dose escalation, would you be specifying tumor types of interest to serve as the basis of an initial – of an initial trial there?

Henry?

Yes, Stephen. Yes, you can see how compelling that study is, because the data was shown preliminary antitumor activity of COM701 alone in patients who are refractory to standard of care therapies including immune checkpoints and also in combination with nuvo in patients who are relapsed following nuvo therapy. You can see that we will be interested in testing a regimen that is PD1 or PD-L1 free just based on the hypothesis that we have. So we haven’t enumerated the tumor types yet. But we’ll be in tumor types that we think will have the high probability of having activity with the inhibition of the two non-redundant parallel pathways.

And Stephen, we will initiate a study – the study is expected to be initiated in the second half of this year.

Wonderful. Thank you for taking the questions and congratulations on the progress.

Thank you.

The next question is from Mark Breidenbach of Oppenheimer. Please go ahead.

Hey. Thanks for taking my questions and congrats on the very encouraging clinical update. This might be a little bit of a rephrasing of one of the questions that was earlier in the queue. But, I am trying to get a sense for, if you have any predictions about specific biomarkers that might indicate cases where the doublet combination might be more suitable than the triplet combination? And I am also wondering if the doublet extension cohorts will test – will include non-small cell lung cancer, which I believe is being included in the triplet study?

So, I’ll start with data and then I’ll let Eran add. I’ll just say, that in general and you are looking from the indications perspective, but in general, from our perspective, the triplet study is the ultimate way for us to test our hypothesis. But now, being in the situation that we are the first to move ahead with PVRIG and now with the data that we have and some initial data supporting the hypothesis, for us now is the time to move ahead and – the clinical strategy and test all the different combinations that are relevant out of this three pathway story. So, we think based on our data and Eran, will relate it that different patient populations with different dominance of these pathways may respond differently. But it is also important for us to have some overlapping indications and this is in order to be able to do some biomarker work and better understand the biology of the PVRIG axis the contribution of the components, how the different patient subsets are responding. So, I think that when you think about the strategy and you think about the different combinations, array of combinations that we are going to execute, and about the different indications, we are also rationally designing how we are going to collect the information out of this patient populations and make eventually decisions about specific subsets that would fit the different combinations. So, with that, I’ll let Eran discuss specifically the doublet versus triplet on patient and data.

Yes. So, basically, all the three pathways has a multiple approach to look at them. We have the ligands of the receptors. We have the expression but different cell types for each of those and then, we do identify some indications and even inside a specific indication from patients which have different dominance across cell types of the different pathways. And, yes, there could be various patients in which the PD1 and these pathways are more dominant and we expect to see more dominant response in these patients even they have sufficient to look at. So, when you look at these in the trial, when you look also at biomarkers, the interim access PD1, et cetera. And second to correlate, if we see these responses, specifically in these patients that we anticipate to response even in the absence of booking.

Okay. That’s helpful. Just another question related to kinetics at response maybe for Henry. Just can you remind us what the average time to response has been across the various cohorts combination or monotherapy cohorts that you see the responses in excluding the one complete response, that got developed nine months in? Thanks

Yes. So, the – like I said, the complete response, the patient with AML squamous cell carcinoma was nine months in until we observed the first complete response. The patient with colorectal cancer microsatellite stable was seven months in, until we saw the first partial response in that patient. Remember, we reduced this here with 0.3 mg per kg body weight and 360 milligrams IV Q 3 weeks of nivolumab. For the patients with primary peritoneal cancer on the monotherapy arm, the partial response was observed at the very first imaging assessment which was at eight weeks. So, you can see, that’s why, I mentioned previously that perhaps it takes much longer in the patient population that is treated for there to be penetration into the tumor itself and that’s where we probably observe that partial response at the outset with the patient with primarily peritoneal cancer and we did see that effect also. So that’s actually ones we are seeing. For the patients with stable disease, it’s obviously at the very first disease assessment and for those who have confirmed stable disease, that stable disease just shows, if you look at the patients with target lesions continuous stabilization in most of these patients and that’s all I can say at this point.

Okay. Fair enough. That’s very helpful.

I would just add for everyone that the corporate presentation is updated with few slides from – describing this clinical data.

Okay. Terrific. Thanks so much for taking my questions.

The next question is from Reni Benjamin of JMP securities. Please go ahead.

Very good morning guys. Thanks for taking the questions and congrats on the update. Maybe just a couple of questions. One, can you just comment on what the median duration of responses across maybe the monotherapy and the combination studies or separately? Also, is there any way outside of the biomarker data to try to narrow down the indications to focus on? I guess, I am trying to get a sense as to how you might be thinking about a registration strategy going forward. And you mentioned other combinations outside of COM701 plus Opdivo, want to just get your thoughts on what sort of combinations you might be thinking about and when you might start those?

Henry, I guess, you’ll take this one.

Yes. I’ll take the question. Hi, Reni. Thank you for your questions. Yes, so, with respect to the median duration of response, we actually haven’t even reached the median for – I mean, it’s still ongoing, because the patient – none of the patients with the exception of the patient with microsatellite stable colorectal cancer that was on for 44 weeks, right. The other two patients are ongoing. So, statistically, the only way to interpret that kind of data is just to say that it’s still not esteemable in terms of the what the median will be, because we have one patient that started treatment now with a complete response, with a confirmed complete response that’s ongoing for 18 months. And then we have the other patients with primary peritoneal cancer that’s ongoing now for 14 months. So, it’s – you got that there, because of the data, it’s heavily skewed towards the patients that are ongoing. It is still too early to know what the median duration of the response will be. However, what one can see from this data is, it’s going to be much longer. It looks like, it’s going to be a much longer than at least a year. So that’s just the preliminary way to look at that in terms of the responders on the study. All right. And then, the other question you asked was, what is our thinking with regards to biomarkers for the indications. That is something that, maybe, Anat and I will probably contribute a little to. We would look at what the expression of these candidate biomarkers are to see if there is any correlation and that will then guide, based on that what the tumor types, whether it’s going to be a basket trial or other kind of innovative trial. With respect to my comments on additional testing outside of immune checkpoint, I think that is a valid way to look at the totality of the safety – the preliminary safety and tolerability profile of COM701. It’s tolerable at the doses that was going as high as 20 mg per kg body weight IV Q 4 weeks. It is tolerable at that dose with nuvo at standard dose is 42 milligrams for IV Q four weeks. I don’t see I foresee if we combine, for example with standard of care therapies in any of the tumor types that we were enumerated, any safety findings. So, it’s still an open question with regards to what’s in those combinations will be and what these tumor types will be and once we get full information, I am not will be able to provide that to you.

Right. Yes, I think that just in terms of the – we are now focusing on the combinations in specific indications and this is why there is some overlap between the indications. We want to make sure that we cover these indications that were raised by our DNAM axis hypothesis and different transitional data, but obviously, focusing on specific indications and taking a path to registrational is something in our mind, and as Henry said, as we move forward, when we formulated this path forward, we’ll share it with the investors.

Okay. And just as a follow-up. We tend to biomarker analyses and quite a bit of analyses on the patients that are responding. Any work that you guys are doing on the patients that aren’t responding? And any learnings that you are obtaining from those that are not responding that you might be able to utilize as an exclusion criteria?

Yes. So we are looking obviously, at all the patients, actually it’s very important as you mentioned to look also in all responding patients and we are correlating all parameters from a – again from a – we are doing all analysis to all the patients and so, all the samples that we have pre and post. And we are going to correlate the biomarkers to respond and of course we are going to also identify the non-responding population to try to understand which patient we should not treat.

Got it. Thanks for taking the questions.

The next question is from Asthika Goonewardene of Truist Securities. Please go ahead.

Hi. Good afternoon guys and congrats on the updates that you provided on the call today. Really exciting to see that. I was wondering maybe another rephrasing of a previous question, but maybe I’ll ask in a different way here. Could you discuss the translational data that gave the confidence that the doublet COM701 Opdivo has sufficient activity in breast, ovarian, endometrial and CLC? I am specifically, wondering what is it that you saw in the data that made you pull the trigger. And I got a couple of follow-ups after that.

So, in terms of translational data, what we start to see is that COM701 is probably inducing enhanced immunity in this regarding the – in the peripheral blood. You can see increase in cytokines, proliferation, et cetera indicating activity. You can see this in monotherapy, which is of course very important to relate to the activity to COM701 itself. We also see this in the combination, again in the COM701 in combination with Opdivo enhanced immune activity and taking this with the clinical data and the clinical response that we’ve seen in the doublet specifically, probably all of this together is strongly hinting for a signal in doublets that should further be explored in clinical studies.

Got it. Thank you, Eran. And then, maybe to Henry, in the expansion study in the prior tumor types, I know that the details are going to be hopefully at ASCO, but I was wondering if you could entertain, how many of these testing were in PD-L1 low or PD-L1 negative tumors? If you can just maybe give us some sort of a sense to that and perhaps if any of them were non-small cell lung cancer patients were PD-L1 low or negative too?

Yes. We will provide that data at ASCO. But I think the key takeaway is, sure, I will not be able to disclose to you now what the analysis in terms of the breakdown was the number of prior therapies, the PD1, PD-L1 percentages are and in terms of consensus with refractory disease and so on. This we will provide in a subsequent release when we update the data. I think what is exciting for us is that, especially in the patient population that we are enrolled on this study in the monotherapy expansion, these are patients who have exhausted all available standard of care therapies. So, it’s not the first-line or second-line. This is just at everything in terms of what the – in the protocol is. Now, it’s also important to note that, like I mentioned of the 20 patients that we have, six have at least stable disease at the time of the previous presentation. So, the breakout will provide that when we update the data.

Got it. And then, lastly, Anat, I was wondering if you could maybe tell us a little bit about when we could see more on your myeloid program and maybe other new applications off the discovery platform? Thanks a lot.

Sure. And so, first I will just make sure that everyone also heard the fact that we are anticipating to disclose additional data also beyond ASCO for the triplet dose escalation in Q4 and also for our COM902 program in Q4. And with respect to myeloid programs, as well as discovery capabilities, we didn’t give any guidance. The guidance is the following for the myeloid programs and for the other programs in our early-stage pipeline. It’s not only including myeloid, but we would like – these are novel programs. We would like to have the science deepening away that we can push this program forward and know that we have a path to the clinic and that we can protect these programs also business-wise. And that’s what’s directing our decisions when and what we are going to disclose. So, with this I know that this is of interest to investors and we will share data as soon as we will get to this point that I just defined. For the computational discovery capabilities, I can only say that we continue to enhance these capabilities. Obviously, there is a huge interest in the computational biology field in the industry. We continue to enhance our capabilities in order to continue to feed our own pipeline. And usually, we are not sharing data with respect to new drug products that we discover at this point in time. So, I think that – and only sharing this type of platforms that we discover, et cetera, but I guess that, with respect to new drug products that we discovered that will need to be – and it remain undisclosed from a corporate strategy.

Thank you very much guys.

Thank you .

The next question is from Tony Butler of ROTH Capital. Please go ahead.

Thanks very much. Just three brief questions if I may. Number one is, when you combine 701, and/or nuvo with 902, 902 when you, in the future do that, 902, as you laid out, dosed Q3 and obviously the other two could be dosed Q4. So I am curious how you think about that if at all today. Number two is, you’ve made comments about some tumor types including breast, which I assume this negative breast. But what’s interesting I think is that 701 has activity, obviously, has been demonstrated in PD-L1 low, PD-L1 negative cohorts. It’s interesting to note that certainly in triple negative breast that only PD1 to immediate voiced and PD-L1 high, so I was just curious given any thought about – because in combination it may have some no noise responses sort of on the PD-L1 negative patients. And then, finally, when you present data at – when data are presented later at ASCO, have you considered having a call or meeting in conjunction with those data to perhaps expand on the total presentation? Thanks very much.

Thank you. And with respect to ASCO, obviously, we first need to get accepted and that we’ll see how to – how we present data as part of the ASCO. So that still remains to be – first need to get accepted. And with respect to the breast and the question with respect to breast or triple negative breast, I’ll just let Henry address it. Henry?

Yes. Thank you so much, Anat. I was on mute. Yes, patients who have triple negative breast cancer eligible for enrollment on to this study. So it’s open to them and I am aware – we are all aware of the data with the PD1/PD-L1 inhibitors in this patient population. So, that’s patients are eligible for enrollment on to this study. Yes, the other question you asked has to do with the dosing strategy in terms of the PK. So, just to give back a little bit, so we have looked at COM701 and this data is already released at both AACR most recently last year. On looking at Q3 dosing and Q4 dosing for COM701and we are able to dose COM701 at any of this – as at Q 3 weeks or Q 4 weeks. For now, the dosing for COM902 is Q 3 weeks, but obviously, we will look to see as we accumulate more data whether dosing can be spaced out to Q4 or any other dosing strategy and this results and what we will do will be based on what the PK data actually shows or which we will obtain and then be able to dose. But having said that, if you recall that, even if there is a difference in terms of dosing, Q 3 weeks, Q 4 for any of the therapy, you can still do evaluation for during dose escalation, evaluate the dosing doesn’t match. You can see many regimens with chemotherapy or even with some of the immune checkpoints where they are combined with other agents to employ that strategy. But, yes, it is a little bit more convenient for patients. It’s two or more agents I administrate have this thing schedule in terms of all the dosing.

Henry, thank you very much and I appreciate.

This concludes our Q&A session. I will now turn the call back to Compugen's President and CEO, Dr. Cohen-Dayag. Would you like to make your concluding statement?

Yes. Thank you. We are enthusiastic by the steady progress and execution across multiple clinical programs, which we believe solidifies Compugen as the leader in DNAM axis immunotherapy. We are excited by the COM701 data we disclosed earlier today, which reinforced our conviction with respect to our clinical development strategy. We look forward to expanding our clinical program to explore additional combination regimens, as well as important data readouts across our ongoing clinical programs evaluating the single, dual, and triple blockade of DNAM axis members. 2021 is expected to provide meaningful insights into the underlying biology and potentially further substantiating the clinical relevance of this axis and with our wholly-owned PVRIG and TIGIT assets, we are uniquely capable of developing potentially transformative cancer immunotherapies. Thank you for joining us today and your continued support. Stay safe and healthy.

Thank you. This concludes the Compugen Limited fourth quarter and full year 2020 financial results conference call. Thank you for your participation. You may go ahead and disconnect.